NUTR 515 Lecture 2 - Obesity

Exam 1

obesity

very high amount of body fat in relation to lean body mass or BMI > 30

no complications

stage 0 of obesity

mild/moderate complications

stage 1 of obesity

severe complications

stage 2 of obesity

women, 40-59

severe obesity continues to rise, especially among —- and those —- years old

BMI 30-34.9

class I of obesity

BMI 35-39.9

class II of obesity

BMI >40

class III of obesity

peripheral and central

fat distribution of hyperplastic obesity

increase cell number and size

adipose cellularity of hyperplastic obesity

related to cell size

insulin resistance of hyperplastic obesity

related to cell size

metabolic consequences of hyperplastic obesity

poor

long term response to prescription in hyperplastic obesity

central

fat distribution in hypertrophic obesity

increased cell size only

adipose cellularity in hypertrophic obesity

related to cell size

insulin resistance in hypertrophic obesity

related to cell size

metabolic consequences in hypertrophic obesity

fair

long term response to prescription in hypertrophic obesity

2x

inducing obesity requires —- amount of kcals to maintain obesity

1/2

spontaneous obese adults require —- as many kcal to maintain obesity than induced

gynoid

fat distribution that is mainly subcutaneous

pear shape

not associated with disease

android

fat distribution that is mainly visceral and subcutaneous

apple shape

0.9

WHR greater than what is considered obese in men

0.85

WHR greater than what is considered obese in women

subcutaneous

fat under skin

visceral

fat between organs

ectopic

fat in lean organs like heart, liver, pancreas, skeletal muscle

appetite

response to thought, sight, smell, taste of food that initiates or delays eating

hunger

physiological drive for food that initiates food seeking behaviors; felt after prolonged deprivation of food

satiety

feeling of satisfaction that inhibits further eating of a meal; determines inter meal time

satiety, adiposity, neural circuits

3 categories of signals between brain and food intake

satiety signals

signals generated in GI tract during meals that initiate satiation and contribute to stopping

adiposity signals

hormonal signals whose secretion is proportional to body fat and decrease food intake and body weight by stimulating receptors locally in brain

neural circuits

in brain that utilize multiple neurotransmitters to integrate signals and cause net catabolic or anabolic responses

lifelong

history in hyperplastic obesity

adult onset

history in hypertrophic obesity

shrink

obese adults can only —- cells, they cannot lose them

glucocorticoids, satiety peptides, insulin, leptin

signals that act on the brain to influence food intake

social and learned factors

meal initiation is based upon — & —-, not so much metabolic or hormonal signals

activate receptors on vagal afferent fibers or stimulate hindbrain directly

types of actions of satiety signals

glucagon, CCK

these satiety signals activate receptors on vagal afferent fibers passing to hindbrain, specifically the nucleus tractus solitarius (NTS)

amylin

this satiety signal stimulates the hindbrain directly

physiological events

CCK released by small intestine is induced by —-

distention and nutrients

physiological events that trigger CCK release

increase

neuropeptide Y does what to food intake

decrease

CCK does what to food intake

decrease

glucagon does what to food intake

increase

ghrelin does what to food intake

adiposity signals

need to know amount of fat stored in the body to regulate weight

neuropeptide Y, CCK, glucagon, amylin, AgRP, ghrelin

important neuronal/hormonal satiety signals

insulin

secreted by pancreatic beta cells in response to circulating glucose, amino acids, fatty acids

amount secreted proportional to body fat (size of fat mass)

leptin

secreted from white adipose cells in response to ongoing metabolic activity of cell

amount secreted proportional to amount of body fat

hypothalamic arcuate nucleus

where there are neurons that synthesize POMC, CART, NPY, AgRP

stimulate

insulin and leptin —- POMC and CART

inhibit

insulin and leptin — NPY/AgRP neurons in arcuate nucleus

alpha MSH

POMC/CART stimulation via leptin/insulin increases —- concentration that act through MC4-R to influence food intake

decrease food intake, increase energy expenditure, decrease body weight

result of stimulation of POMC/CART and increase of aMSH

increase intake, decrease energy expenditure, increase body weight

NPY acts in the hypothalamus to —-

antagonist

AgRP is an — of MC4-R and can block actions of aMSH

increase intake

result of AgRP action

NPY, POMC, MSH

mediators of leptin

secretion is proportional to body fat, able to acquire access to brain, receptors in hypothalamus, increase signaling and decrease intake and vice versa

adiposity hormone criteria

predispose, determines expression

genetics —, environment — —

leptin, leptin receptor, POMC, PCSKI

autosomal recessive single gene mutations associated with obesity

MC4R

autosomal dominant single gene mutations associated with obesity

behavioral modification, pharmacological, surgical treatment

treatment for obesity

BMI >40 or 35-40 with significant comorbidities, unsuccessful weight loss, clearance, no medical contraindications to surgery

indications for surgical treatment of obesity

roux en y, duodenal switch, vertical banded gastroplasty, laparoscopic adjustable gastric band

types of bariatric surgery

roux en y

reroute small intestine to upper stomach to make stomach smaller

bypass pyloric valve and duodenum

duodenal switch

take out part of the stomach and reroute intestine

vertical banded gastroplasty

make stomach smaller without doing anything to intestine, similar to roux en y

laparoscopic adjustable gastric band

make stomach smaller by putting band around upper portion

can get gastritis

25-35%

long term weight loss expectations for roux en y

20-30%

long term weight loss expectations for sleeve

30-40%

long term weight loss expectations for duodenal switch

malabsorption, micronutrient deficiencies

side effects that are profound in bariatric surgery

cure of insulin resistance within 5-7 days after surgery

unexpected benefit of bariatric surgery

copper, iodine

what is absorbed in stomach

iron, zinc, riboflavin, biotin, copper, selenium, folate, calcium, thiamin, niacin, vitamin a, e, k

what is absorbed in duodenum

zinc, calcium, manganese, pyridoxine, vitamin c, selenium, chromium, thiamin, folate, pantothenate, iron, riboflavin, niacin, vitamin a, d, e, k

what is absorbed in the jejunum

folate, vitamin c, d, k, b12

what is absorbed in the ileum

orexigenic

those that coexpress NPY/AgRP are known as what

anorexigenic

those that coexpress POMC/CART are known as what